The Cardiovascular System

Chapter 20

The Heart

Location

The heart lies in the mediastinum.

Pericardium and Layers of Heart Wall

Chambers and Sulci

Chambers and Sulci

Right Atrium

Right Ventricle

Left Atrium

Left Ventricle

Anterior Heart

Myocardial Thickness and FunctionThickness of myocardium varies according to the function of the chamber

Atrioventricular Valves

• Blood flow– Blue: deoxygenated– Red: oxygenated

Blood Circulation

Coronary Circulation

Coronary Artery Disease

Coronary Artery Disease

Coronary Artery Disease

Cardiac Muscle Histology

Conducting System

Autorhythmic cells – self excitableReduced permeability of K+, but no change in permeability to Na+.

Na+ continues to diffuse in.

Unstable resting potential – continuously depolarizes, drifting slowly toward threshold. (pacemaker potential)

Physiology of ContractionPotentials initiated by conducting fibers stimulate contractile fibers.

Electrocardiogram (ECG/EKG)

EKG

Cardiac Rhythm and Rate

Normal heart rate: 60-100 beats/min

Avg. heart beat at rest: 70-72 beats/min

Sinus tachycardia: > 100 beats/min

Sinus bradycardia: < 60 beats/min

Cardiac Rhythm and RateArrhythmias: abnormal rhythm resulting from a defect in the

heart conduction system.

Fibrillation: rapid and irregular contractions. Can be atrial or ventricular.

Defibrillation: electrical shock to depolarize myocardium.

Ectopic Focus: a region of the heart, other than the conducting system, that causes and abnormal depolarization.

Junctional rhythm: AV node becomes pacemaker

Heart block: an arrhythmia that occurs when electrical pathway between the atria and ventricle is blocked.

EKG

Cardiac

CycleSystole: contraction

Diastole: relaxation

Heart soundsLubb - AV valves close Dupp - semilunar valves close

Stroke Volume (SV)

EDV = Amount of blood that collects in a ventricle during diastole

ESV = Amount of blood remaining in a ventricle after contraction

Stroke volume = end diastolic volume - end systolic volume

SV = EDV - ESV

SV depends on amount of stretch produced by venous return.

Averages about 70 ml/beat

Anything that influences heart rate or blood volume influences venous return and therefore SV

Volume of blood pumped out by a ventricle with each beat

Cardiac Output (CO)

Cardiac output = Heart rate x Stroke volume

HR = beats per minute

SV = volume of blood pumped out by a ventricle with each beat

CO = HR x SV

amount of blood pumped by each ventricle in one minute

– Degree of stretch on the heart before it contracts– Greater preload increases the force of contraction– Frank-Starling law of the heart – the more the

heart fills with blood during diastole, the greater the force of contraction during systole

• Preload proportional to end-diastolic volume (EDV)

– 2 factors determine EDV1. Duration of ventricular diastole2. Venous return – volume of blood returning to right

ventricle

Factors Affecting SVPreload

– Strength of contraction at any given preload– Positive inotropic agents increase contractility

• Often promote Ca2+ inflow during cardiac action potential

• Increases stroke volume

• Epinephrine, norepinephrine, digitalis

– Negative inotropic agents decrease contractility• Anoxia, acidosis, some anesthetics, and increased K+ in

interstitial fluid

ContractilityFactors Affecting SV

– Pressure that must be overcome before a semilunar valve can open

– Increase in afterload causes stroke volume to decrease

• Blood remains in ventricle at the end of systole

– Hypertension and atherosclerosis increase afterload

Afterload

Factors Affecting SV

Regulation of Heart Rate

2. Chemical regulation

3. Other Factors

1. Autonomic regulation

Change stroke volume and/or heart rate

Cardiac Output

Homeostatic Imbalance of CO

Congestive heart failure - occurs when the pumping ability of the heart is inadequate to provide normal circulation to meet body needs.

Pulmonary congestion - left side failure

Peripheral congestion - right side failure